Introduction of GRIN2A
Glutamate receptor ionotropic, NMDA 2A (GRIN2A) is a subunit of the NMDA receptors. This protein in humans is encoded by the GRIN2A gene. It can form di-heteromers or tri-heteromers with the other subunits such as GRIN1, GRIN2B, GRIN2C, GRIN2D, or GRIN3 to generate functional NMDARs. Structurally, GRIN2A has three transmembrane segments and a reentrant pore loop. GRIN2A expression is ubiquitous in the central nervous system (CNS), starting at very low levels around the time of birth, and increasing dramatically during the second postnatal week. During the second postnatal week, GRIN2A replaces GRIN2B as the primary GRIN2 subunit at synaptic sites in the cortex and hippocampus. Through the C-termini of GRIN2A, it can interact with multiple intracellular proteins to mediate multiple physiological functions. However, many of the molecular mechanisms regulating GRIN2A trafficking remain to be elucidated.
|Basic Information of GRIN2A|
|Protein Name||Glutamate receptor ionotropic, NMDA 2A|
|Gene Name||GRIN2A, NMDAR2A|
|Aliases||NMDAR2A, NR2A, hNR2A|
|Organism||Homo sapiens (Human)|
Functions of GRIN2A Membrane Protein
GRIN2A proteins are highly expressed in the cortex and hippocampus, and play a critical role in the synaptic function by controlling synaptic plasticity and metaplasticity. However, the exact role of GRIN2A in long-term potentiation and long-term depression is still controversial. Besides, studies in mice lacking the GRIN2A have demonstrated that it is also involved in learning and memory. Moreover, GRIN2A is implicated in different human neurological diseases and disorders, such as cerebral ischemia, seizure disorder, Alzheimer's disease, schizophrenia, Parkinson’s disease, and systemic lupus erythematosus. However, the causality between GRIN2A and these brain diseases has not been determined. Moreover, only a small number of reports have suggested treatment strategies based on GRIN2A or its signaling pathways. The pharmacological potential of this protein remains to be further explored in the future.
Application of GRIN2A Membrane Protein in Literature
This study investigated the contribution of GluN2A subunit to synaptic plasticity and learning in GluN2A knockout, heterozygous, and wild-type mice.
This article investigated the distribution of GluN2A and GluN2B subunits from L5 neurons of wild-type and GluN2A-deficient mice, using focal laser scanning photostimulation of caged glutamate, slice electrophysiology, and small peptide antagonists.
This article described the identification of positive allosteric modulators (PAMs) of NMDARs with selectivity for GluN2A-containing receptors.
This article reported a group of pyrazine-containing GluN2A antagonists, such as MPX-004 and MPX-007. The selectivity and potency were studied. The results showed these antagonists were highly selective pharmacological probes to explore the physiology and their therapeutic potential.
This article reported that auditory fear memories created with 10 tone-shock pairings were resistant to retrieval-dependent memory destabilization and were associated with an increase in the synaptic GluN2A/GluN2B ratio in neurons of the basal and lateral amygdala (BLA) compared with weaker fear memories created via one or three tone-shock pairings.
GRIN2A Preparation Options
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